NF1 is a GTPase activating protein (GAP) that negatively regulates the activity of Ras by accelerating the conversion rate of Ras-bound GTP to GDP via GTP hydrolysis. Loss of functional NF1 protein due to mutations in the NF1 gene causes the autosomal dominant disorder neurofibromatosis type 1 (NF1) (1). Children with NF1 will develop tumors throughout their lifetime, with tumor frequency increasing as they age. Plexiform neurofibromas (PNs) pose the greatest threat to NF1 patients, as they can transform into malignant peripheral nerve sheath tumors (MPNSTs), highly resistant sarcomas with a 5-year survival of 16-38% (2-4). NF1 loss is also considered contributive to the development of aggressive neurological cancers, including glioblastoma and neuroblastoma (5-7). While there are clinical trials investigating new therapies for NF1 deficient PNs and MPNSTs, such as MEK inhibitor therapy, PD-1-targeted immunotherapy, and mTOR inhibitor combination therapy, there still exists a critical need for novel therapeutics (8-12).